The α2Na+/K+-ATPase is critical for skeletal and heart muscle function in zebrafish

Canan Doganli; Kasper Kjaer-Sørensen; Christopher Knoeckel; Hans Christian Beck; Jens Randel Nyengaard; Bent Honoré; Poul Nissen; Angela Ribera; Claus Oxvig; Karin Lykke-Hartmann

doi:10.1242/jcs.115808

The α₂Na⁺/K⁺-ATPase is critical for skeletal and heart muscle function in zebrafish

Canan Doganli, Kasper Kjaer-Sørensen, Christopher Knoeckel, Hans Christian Beck, Jens Randel Nyengaard, Bent Honoré, Poul Nissen, Angela Ribera, Claus Oxvig, Karin Lykke-Hartmann

Research output: Contribution to journal/Conference contribution in journal/Contribution to newspaper › Journal article › Research › peer-review

20 Citations (Scopus)

Abstract

The Na⁺/K⁺-ATPase generates ion gradients across the plasma membrane, essential for multiple cellular functions. In mammals, four different Na⁺/K⁺-ATPase α-subunit isoforms are associated with characteristic cell-type expression profiles and kinetics. We found the zebrafish α₂Na⁺/K⁺-ATPase associated with striated muscles and that α₂Na⁺/K⁺-ATPase knockdown causes a significant depolarization of the resting membrane potential in slow-twitch fibers of skeletal muscles. Abrupt mechanosensory responses were observed in α₂Na⁺/K⁺-ATPase deficient embryos, possibly linked to a postsynaptic defect. The α₂Na⁺/K⁺-ATPase deficiency reduced the heart rate and caused a loss of left-right asymmetry in the heart tube. Similar phenotypes observed by knockdown of the Na⁺/Ca^₂+ exchanger indicated a role for the interplay between these two proteins on the observed phenotypes. Furthermore, proteomics identified up- and down-regulation of specific phenotype-related proteins, such as parvalbumin, CaM, GFAP and multiple kinases, thus highlighting a potential proteome change associated with the dynamics of α₂Na⁺/K⁺-ATPase. Taken together, our findings display that zebrafish α₂Na⁺/K⁺-ATPase is important for skeletal and heart muscle functions

Original language	English
Journal	Journal of Cell Science
Volume	125
Pages (from-to)	6166-6175
Number of pages	10
ISSN	0021-9533
DOIs	https://doi.org/10.1242/jcs.115808
Publication status	Published - Dec 2012

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10.1242/jcs.115808

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@article{37e2ada46f3d42fd8752b0cbd66bf111,

title = "The α2Na+/K+-ATPase is critical for skeletal and heart muscle function in zebrafish",

abstract = "The Na+/K+-ATPase generates ion gradients across the plasma membrane, essential for multiple cellular functions. In mammals, four different Na+/K+-ATPase α-subunit isoforms are associated with characteristic cell-type expression profiles and kinetics. We found the zebrafish α2Na+/K+-ATPase associated with striated muscles and that α2Na+/K+-ATPase knockdown causes a significant depolarization of the resting membrane potential in slow-twitch fibers of skeletal muscles. Abrupt mechanosensory responses were observed in α2Na+/K+-ATPase deficient embryos, possibly linked to a postsynaptic defect. The α2Na+/K+-ATPase deficiency reduced the heart rate and caused a loss of left-right asymmetry in the heart tube. Similar phenotypes observed by knockdown of the Na+/Ca2+ exchanger indicated a role for the interplay between these two proteins on the observed phenotypes. Furthermore, proteomics identified up- and down-regulation of specific phenotype-related proteins, such as parvalbumin, CaM, GFAP and multiple kinases, thus highlighting a potential proteome change associated with the dynamics of α2Na+/K+-ATPase. Taken together, our findings display that zebrafish α2Na+/K+-ATPase is important for skeletal and heart muscle functions",

author = "Canan Doganli and Kasper Kjaer-S{\o}rensen and Christopher Knoeckel and Beck, {Hans Christian} and Nyengaard, {Jens Randel} and Bent Honor{\'e} and Poul Nissen and Angela Ribera and Claus Oxvig and Karin Lykke-Hartmann",

year = "2012",

month = dec,

doi = "10.1242/jcs.115808",

language = "English",

volume = "125",

pages = "6166--6175",

journal = "Journal of Cell Science",

issn = "0021-9533",

publisher = "Company of Biologists Ltd",

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T1 - The α2Na+/K+-ATPase is critical for skeletal and heart muscle function in zebrafish

AU - Doganli, Canan

AU - Kjaer-Sørensen, Kasper

AU - Knoeckel, Christopher

AU - Beck, Hans Christian

AU - Nyengaard, Jens Randel

AU - Honoré, Bent

AU - Nissen, Poul

AU - Ribera, Angela

AU - Oxvig, Claus

AU - Lykke-Hartmann, Karin

PY - 2012/12

Y1 - 2012/12

N2 - The Na+/K+-ATPase generates ion gradients across the plasma membrane, essential for multiple cellular functions. In mammals, four different Na+/K+-ATPase α-subunit isoforms are associated with characteristic cell-type expression profiles and kinetics. We found the zebrafish α2Na+/K+-ATPase associated with striated muscles and that α2Na+/K+-ATPase knockdown causes a significant depolarization of the resting membrane potential in slow-twitch fibers of skeletal muscles. Abrupt mechanosensory responses were observed in α2Na+/K+-ATPase deficient embryos, possibly linked to a postsynaptic defect. The α2Na+/K+-ATPase deficiency reduced the heart rate and caused a loss of left-right asymmetry in the heart tube. Similar phenotypes observed by knockdown of the Na+/Ca2+ exchanger indicated a role for the interplay between these two proteins on the observed phenotypes. Furthermore, proteomics identified up- and down-regulation of specific phenotype-related proteins, such as parvalbumin, CaM, GFAP and multiple kinases, thus highlighting a potential proteome change associated with the dynamics of α2Na+/K+-ATPase. Taken together, our findings display that zebrafish α2Na+/K+-ATPase is important for skeletal and heart muscle functions

AB - The Na+/K+-ATPase generates ion gradients across the plasma membrane, essential for multiple cellular functions. In mammals, four different Na+/K+-ATPase α-subunit isoforms are associated with characteristic cell-type expression profiles and kinetics. We found the zebrafish α2Na+/K+-ATPase associated with striated muscles and that α2Na+/K+-ATPase knockdown causes a significant depolarization of the resting membrane potential in slow-twitch fibers of skeletal muscles. Abrupt mechanosensory responses were observed in α2Na+/K+-ATPase deficient embryos, possibly linked to a postsynaptic defect. The α2Na+/K+-ATPase deficiency reduced the heart rate and caused a loss of left-right asymmetry in the heart tube. Similar phenotypes observed by knockdown of the Na+/Ca2+ exchanger indicated a role for the interplay between these two proteins on the observed phenotypes. Furthermore, proteomics identified up- and down-regulation of specific phenotype-related proteins, such as parvalbumin, CaM, GFAP and multiple kinases, thus highlighting a potential proteome change associated with the dynamics of α2Na+/K+-ATPase. Taken together, our findings display that zebrafish α2Na+/K+-ATPase is important for skeletal and heart muscle functions

U2 - 10.1242/jcs.115808

DO - 10.1242/jcs.115808

M3 - Journal article

C2 - 23097043

SN - 0021-9533

VL - 125

SP - 6166

EP - 6175

JO - Journal of Cell Science

JF - Journal of Cell Science

ER -

The α2Na+/K+-ATPase is critical for skeletal and heart muscle function in zebrafish

Abstract

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The α₂Na⁺/K⁺-ATPase is critical for skeletal and heart muscle function in zebrafish